A genetical basis of repair deficiency has been reported principally in two types of human-derived cells, in xeroderma pigmentosum and ataxia telangiectasia cells. In general, however, the molecular biology underlying radiation response, and how it is influenced by repair processes, is less well understood in eucaryotes than in procaryotes; progress with procaryotes has reflected the availability of a number of repair deficient mutants. Recently, a method of producing clones of V79 Chinese hamster cells having heritable, enhanced responses to radiation (ionizing and non-ionizing) was discovered in the applicant's laboratory. V79 Chinese hamster cells resistant to the metabolic inhibitor ouabain (i.e., spontaneous mutants) may be classified as small- and as large-colony formers. The latter appear to have normal radiation responses while the former generally have enhanced responses. Thus, the metabolic impairment(s) made evident by reduced colony size appears to be tightly coupled to radiation responsiveness. Using the methods of somatic-cell hybridization, a genetical basis will be sought for repair deficient cells. While the research will involve a number of seconary objectives, the primary one will be to see if complementation groups exist relative to repair processes among clonal isolates having different radiation responsivenesses. Hybrids from different small-colony formers, which yield "wild type" responses, will be assumed to represent different genetic complementation groups. A hybrid between a (sensitive) small-colony former and a (resistant) large-colony former, which has the radiation properties of the former, will be an indication of repression of a repair function. The radiaion responses of hybrids formed from cells from the same clones (small- and large-colony formers) will serve as controls of the influence of hybridization itself.